Reperfusion of the blood flow to ischemic myocardium is the standard treatment for patients suffering myocardial infarction. However, the reperfusion itself can also induce myocardial injury, in which the actual mechanism and its risk factors remain unclear. This work aims to study the mechanism of ischemia–reperfusion treatment using a three-dimensional (3D) oxygen diffusion model. An electrical model is then coupled to an oxygen model to identify the possible region of myocardial damage. Our findings show that the value of oxygen exceeds its optimum (>1.0) at the ischemic area during early reperfusion period. This complication was exacerbated in a longer ischemic period. While a longer reperfusion time causes a continuous excessive oxygen supply to the ischemic area throughout the reperfusion time. This work also suggests the use of less than 0.8 of initial oxygen concentration in the reperfusion treatment to prevent undesired upsurge at the early reperfusion period and further myocardial injury. We also found the region at risk for myocardial injury is confined in the ischemic vicinity revealed by its electrical conductivity impairment. Although there is a risk that reperfusion leads to myocardial injury for excessive oxygen accumulation, the reperfusion treatment is helpful in reducing the infarct size.

将血流再灌注至缺血性心肌是患有心肌梗塞的患者的标准治疗方法。然而，再灌注本身也可能诱发心肌损伤，其中实际机制及其危险因素尚不清楚。这项工作旨在利用三维（3D）氧扩散模型研究缺血再灌注治疗的机制。然后将电模型与氧模型耦合，以识别心肌损伤的可能区域。我们的研究结果表明，在再灌注早期，缺血区域的氧气值超过了最佳值（> 1.0）。在较长的缺血期，这种并发症会加剧。虽然较长的再灌注时间导致在整个再灌注时间内持续过量的氧气供应到缺血区域。这项工作还建议在再灌注治疗中使用少于0.8的初始氧气浓度，以防止在再灌注早期不希望的高潮和进一步的心肌损伤。我们还发现有心肌损伤危险的区域局限于其电导率受损所揭示的局部缺血区域。尽管存在由于过度氧气积累而导致再灌注导致心肌损伤的风险，但再灌注治疗有助于减小梗塞面积。